Anti-Müllerian Hormone (AMH) May Stall Ovarian Cortex Function Through Modulation of Hormone Receptors Other Than the AMH Receptor

Autor: Laura Detti, Ghassan M. Saed, Nicole M. Fletcher, Rebecca A. Uhlmann, Irene Peregrin-Alvarez
Rok vydání: 2017
Předmět:
0301 basic medicine
Adult
Anti-Mullerian Hormone
endocrine system
medicine.medical_specialty
endocrine system diseases
Ovarian Cortex
Receptors
Peptide
Pilot Projects
Biology
law.invention
Receptor
IGF Type 1
03 medical and health sciences
0302 clinical medicine
law
Internal medicine
medicine
Humans
Inhibins
RNA
Messenger
Receptors
Pituitary Hormone
Receptor
030219 obstetrics & reproductive medicine
Cell growth
Ovary
food and beverages
Obstetrics and Gynecology
Anti-Müllerian hormone
Receptors
Somatomedin
Receptors
LH
female genital diseases and pregnancy complications
Recombinant Proteins
030104 developmental biology
Endocrinology
Gene Expression Regulation
Premenopause
Hormone receptor
biology.protein
Recombinant DNA
Receptors
FSH
Female
AMH receptor
Receptors
Transforming Growth Factor beta
Hormone
Zdroj: Reproductive sciences (Thousand Oaks, Calif.). 25(8)
ISSN: 1933-7205
Popis: To test whether recombinant anti-Müllerian hormone (AMH) can inhibit ovarian cortex function by modulating the expression of other hormone receptors.Pilot experimental study with ovarian cortex obtained from 5 patients. Immediately after explant, the ovarian cortex specimens were divided into 5 equal fragments. One fragment was flash-frozen (uncultured) and 4 were incubated for 48 hours at 37°C in a pH-adjusted gamete buffer medium with increasing AMH concentrations of 0, 5, 25, and 50 ng/mL. After incubation, all specimens were rinsed and flash-frozen for polymerase chain reaction (PCR) executed in triplicates. We utilized real-time reverse transcription-polymerase chain reaction (RT-PCR) to determine messenger RNA (mRNA) levels of AMH and its receptor Anti-Müllerian Hormone-Receptor 2 (AMH-R2), follicle stimulating hormone receptor (FSH-R), luteinizing hormone receptor (LH-R), inhibin B, and insulin-like growth factor 1 receptor 1 (IGF1-R1) in ovarian cortex tissue. In addition, we performed Ki-67 immunostaining to evaluate cell proliferation in the treatment groups.Absence of recombinant human AMH (rAMH) caused upregulation of all markers. Exposure to increasing rAMH concentrations caused tissue AMH expression downregulation ( P = .024), while AMH-R2 ( P = .005), FSH-R ( P = .009), LH-R ( P = .003), and inhibin B ( P = .001) mRNA expression followed a bell-shaped response with an increased expression at low dose, followed by a decreased expression at higher doses. Expression of IGF1-R1 was independent ( P = .039) of rAMH exposure. The Ki-67 immunostaining showed an increased cell proliferation in the media control compared to the uncultured and the tissue cultured with rAMH.Culture with increasing rAMH concentrations caused downregulation of its own, as well as other hormone receptors, and a decreased ovarian cortex cell proliferation. These results help understanding the inhibitory effects of AMH on follicular development.
Databáze: OpenAIRE
Externí odkaz: